Feasibility of Sensor Technology for Balance Assessment in Home Rehabilitation Settings.

The increased use of sensor technology has been crucial in releasing the potential for remote rehabilitation. However, it is vital that human factors, that have potential to affect real-world use, are fully considered before sensors are adopted into remote rehabilitation practice. The smart sensor devices for rehabilitation and connected health (SENDoc) project assesses the human factors associated with sensors for remote rehabilitation of elders in the Northern Periphery of Europe. This article conducts a literature review of human factors and puts forward an objective scoring system to evaluate the feasibility of balance assessment technology for adaption into remote rehabilitation settings. The main factors that must be considered are: Deployment constraints, usability, comfort and accuracy. This article shows that improving accuracy, reliability and validity is the main goal of research focusing on developing novel balance assessment technology. However, other aspects of usability related to human factors such as practicality, comfort and ease of use need further consideration by researchers to help advance the technology to a state where it can be applied in remote rehabilitation settings.

Exploring Self-Repair in a Coupled Spiking Astrocyte Neural Network.

It is now known that astrocytes modulate the activity at the tripartite synapses where indirect signaling via the retrograde messengers, endocannabinoids, leads to a localized self-repairing capability. In this paper, a self-repairing spiking astrocyte neural network (SANN) is proposed to demonstrate a distributed self-repairing capability at the network level. The SANN uses a novel learning rule that combines the spike-timing-dependent plasticity (STDP) and Bienenstock, Cooper, and Munro (BCM) learning rules (hereafter referred to as the BSTDP rule). In this learning rule, the synaptic weight potentiation is not only driven by the temporal difference between the presynaptic and postsynaptic neuron firing times but also by the postsynaptic neuron activity. We will show in this paper that the BSTDP modulates the height of the plasticity window to establish an input-output mapping (in the learning phase) and also maintains this mapping (via self-repair) if synaptic pathways become dysfunctional. It is the functional dependence of postsynaptic neuron firing activity on the height of the plasticity window that underpins how the proposed SANN self-repairs on the fly. The SANN also uses the coupling between the tripartite synapses and γ -GABAergic interneurons. This interaction gives rise to a presynaptic neuron frequency filtering capability that serves to route information, represented as spike trains, to different neurons in the subsequent layers of the SANN. The proposed SANN follows a feedforward architecture with multiple interneuron pathways and astrocytes modulate synaptic activity at the hidden and output neuronal layers. The self-repairing capability will be demonstrated in a robotic obstacle avoidance application, and the simulation results will show that the SANN can maintain learned maneuvers at synaptic fault densities of up to 80% regardless of the fault locations.

GABA Regulation of Burst Firing in Hippocampal Astrocyte Neural Circuit: A Biophysical Model.

It is now widely accepted that glia cells and gamma-aminobutyric acidergic (GABA) interneurons dynamically regulate synaptic transmission and neuronal activity in time and space. This paper presents a biophysical model that captures the interaction between an astrocyte cell, a GABA interneuron and pre/postsynaptic neurons. Specifically, GABA released from a GABA interneuron triggers in astrocytes the release of calcium (Ca 2+) from the endoplasmic reticulum via the inositol 1, 4, 5-trisphosphate (IP 3) pathway. This results in gliotransmission which elevates the presynaptic transmission probability rate (PR) causing weight potentiation and a gradual increase in postsynaptic neuronal firing, that eventually stabilizes. However, by capturing the complex interactions between IP 3, generated from both GABA and the 2-arachidonyl glycerol (2-AG) pathway, and PR, this paper shows that this interaction not only gives rise to an initial weight potentiation phase but also this phase is followed by postsynaptic bursting behavior. Moreover, the model will show that there is a presynaptic frequency range over which burst firing can occur. The proposed model offers a novel cellular level mechanism that may underpin both seizure-like activity and neuronal synchrony across different brain regions.